| Summary: | <p>Abstract</p> <p>Background</p> <p><it>TNFRSF11B </it>computational development network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy.</p> <p>Methods</p> <p>By integration of gene regulatory network infer (GRNInfer) and the database for annotation, visualization and integrated discovery (DAVID) we identified and constructed significant molecule <it>TNFRSF11B </it>development network from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726.</p> <p>Results</p> <p>Our result verified <it>TNFRSF11B </it>developmental process only in the downstream of frontal cortex of HIVE-control patients (<it>BST2, DGKG, GAS1, PDCD4, TGFBR3, VEZF1 </it>inhibition), whereas in the upstream of frontal cortex of HIVE (<it>DGKG, PDCD4 </it>activation) and downstream (<it>CFDP1, DGKG, GAS1, PAX6 </it>activation; <it>BST2, PDCD4, TGFBR3, VEZF1 </it>inhibition). Importantly, we datamined that <it>TNFRSF11B </it>development cluster of HIVE is involved in T-cell mediated immunity, cell projection organization and cell motion (only in HIVE terms) without apoptosis, plasma membrane and kinase activity (only in HIVE-control patients terms), the condition is vital to inflammation, brain morphology and cognition impairment of HIVE. Our result demonstrated that common terms in both HIVE-control patients and HIVE include developmental process, signal transduction, negative regulation of cell proliferation, RNA-binding, zinc-finger, cell development, positive regulation of biological process and cell differentiation.</p> <p>Conclusions</p> <p>We deduced the stronger <it>TNFRSF11B </it>development network in HIVE consistent with our number computation. It would be necessary of the stronger <it>TNFRSF11B </it>development function to inflammation, brain morphology and cognition of HIVE.</p>
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